Temporal bone imaging.

REVIEW ARTICLE

Temporal Bone Imaging Kristen Fruauff, MD, Kristen Coffey, MD, J. Levi Chazen, MD, and C. Douglas Phillips, MD Abstract: Temporal bone imaging is performed for a variety of clinical conditions addressed in the outpatient and acute care setting ranging from hearing loss to trauma. Recent advances in magnetic resonance technology have enhanced the assessment of fine anatomic temporal bone detail and improved the diagnostic sensitivity for important pathology. For example, non–echo planar diffusion weighted imaging increases detection rate and diagnostic confidence of recurrent cholesteatoma. This chapter will focus on relevant temporal bone clinical entities and new MR developments that have come into clinical practice. Key Words: temporal bone, advanced MR techniques, MRI of the temporal bone, postoperative cholesteastoma, non–echo planar DWI, perineural tumor spread (Top Magn Reson Imaging 2015;24: 39–55)

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emporal bone imaging is performed for a variety of clinical conditions. Hearing loss and vertigo account for the majority of outpatient scans; temporal bone trauma is the most common referral for inpatient imaging. Hearing loss is a common clinical entity, particularly with aging, with presbycusis accounting for the majority of cases in the elderly. Screening recommendations involve questionnaires and whispered-voice test. Patients with subjective hearing loss and those unable to perceive the whispered voice are then evaluated by audiometry to determine the degree of hearing loss and conductive or sensorineural component.1 If a conductive hearing loss (CHL) is detected, high-resolution temporal bone computed tomography (CT) is the study of choice given the excellent bony detail and ability to detect even small osseous abnormalities.2 Sensorineural hearing loss (SNHL) is a more protean clinical condition. Sudden, fluctuating, and progressive SNHL are recognized as subtypes with distinct differential diagnoses. Magnetic resonance imaging (MRI) is the mainstay of imaging evaluation in patients with SNHL. Sudden SNHL may be related to viral infection, vascular disease, inner ear membrane abnormality, or rarely, vestibular schwannoma.3 Contrast administration may help to further differentiate these disease entities. For example, inner ear or cochlear nerve enhancement may indicate viral SNHL with a lower rate of steroid response than MRI-negative sudden SNHL.4 Fluctuating SNHL is a challenge diagnostically—enlarged vestibular aqueduct and Meniere disease are the two most prevalent diagnoses with fluctuating SNHL. These conditions will be discussed in detail and may be distinguished by age at presentation; the majority of enlarged vestibular aqueduct patients become symptomatic in childhood.5 The vestibular aqueduct may be reduced in size with Meniere disease. Although traditional MRI has been unrevealing in Meniere disease, newer MR techniques show promise in imaging diagnosis.6 Asymmetric SNHL may be further divided into cochlear and retrocochlear pathologies. For patients with audiometric and auditory brain response testing suggestive of a retrocochlear lesion, contrast MRI of the brain is recommended with thin section constructive interference in steady state (CISS) sequences. From the Weill Cornell Medical College, New York, NY. Reprints: Kristen Fruauff, MD, Weill Cornell Medical College, New York, NY (e‐mail: [email protected]). The authors declare no conflict of interest. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Mixed CHL and SNHL is classically caused by otospongiosis (otosclerosis), for which high-resolution temporal bone CT is the imaging study of choice.5 Other common indications for temporal bone imaging indicative of brainstem, middle, or inner ear pathology are generally best evaluated with high-resolution MRI, for example, congenital hearing loss, tinnitus, dizziness, vertigo, and other vestibular disorders. Computed tomography often plays a complementary role, particularly for surgical planning, but is often not the initial study of choice. These entities will be discussed in detail in the subsequent sections. A number of exciting developments in MRI have come into clinical practice in regard to the internal auditory canal (IAC) and temporal bone. Non–echo planar diffusion-weighted imaging (non-EP DWI) has improved the diagnostic sensitivity and specificity for residual cholesteatoma. Magnetic resonance neurography techniques for cranial nerve imaging has increased the visualization of small IAC branches and enhanced the diagnostic accuracy for cranial nerve pathology.

ADVANCED MR TECHNIQUES High-Resolution T2 Imaging Spin-echo T2-weighted imaging has been the mainstay for imaging of cisternal cranial nerves at the cerebellopontine angles and IACs. The negative contrast illustrated by the brainstem, cisternal cranial nerves, and vascular structures outlines the normal segments against T2-hyperintense cerebrospinal fluid (CSF). Steady-state–free precession (SSFP) heavily T2-weighted imaging enhances cranial nerve visualization over standard spin-echo T2 techniques.7 Three-dimensional (3-D) CISS or 3-D fast imaging using steady state acquisition (FIESTA) are part of a complete posterior fossa and IAC clinical protocol. Given the T1 and T2 echo-balanced nature of SSFP sequences, some authors have advocated contrast-enhanced CISS to further delineate the position of CN VII and VII relative to cisternal masses.8 Cranial nerve visualization may be further enhanced with 3-D turbo spin echo techniques, particularly when driven equilibrium radiofrequency reset pulse (DRIVE) imaging is performed. DRIVE reduces imaging time and pulsation artifact.9

Non–Echo Planar Diffusion Imaging Traditional echo planar diffusion imaging, although rapid and extremely useful in brain imaging, suffers from susceptibility artifact at bone-air interfaces. The susceptibility effect is particularly limiting in the temporal bone. Diffusion imaging is advantageous in many temporal bone cases particularly for cholesteatoma detection in the postoperative setting. To overcome these limitations, non-EP DWI techniques have been developed, allowing thin section acquisition through the temporal bone with marked reduction in susceptibility artifact. Non-EP DWI has high accuracy for postoperative cholesteatoma detection with sensitivity and specificity exceeding 95%.10

Diffusion Tensor Imaging Diffusion tensor imaging has limited utility for evaluation of the VII/VIII cranial nerve complex in a routine clinical setting

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although investigators have shown fiber displacement from cerebellopontine angle schwannomas.11 There are promising developments in imaging other cranial nerves, for example, in trigeminal neuralgia, lower fractional anisotropy values may been seen in the clinically affected nerve.12 Investigations show promise with 3-D PSIF diffusion and CISS techniques of distal facial nerve branches as they ramify through the parotid gland.13

unilocular T1 hypointense and T2 hyperintense lesions. The small sinus tracts can be seen as a T2 hyperintense tract to the skin, EAC, or rarely the parapharyngeal space (Fig. 2).15

MRI Techniques for Bony Detail

Congenital Cholesteatoma

Investigational MRI techniques show potential for delineating fine bony detail, typically a task limited to high-resolution CT imaging. Sweep imaging with Fourier transformation (SWIFT) is one such method described with good results for imaging the mandible.14 SWIFT uses a time-shared excitation to acquire multiple relaxation times including those with markedly short T2. This overcomes the signal decay normally experienced with cortical bone where T2 relaxation times can be as low as 200 microseconds. SWIFT has been applied to the mandible with good image quality (Fig. 1); temporal bone imaging is under investigation.

Cholesteatomas arise from the exfoliation of hyperplastic keratinized epithelium with a resultant surrounding inflammatory stroma.16 Cholesteatomas may be divided into congenital and acquired subtypes. The congenital form is associated with EAC stenosis or atresia.16 A congenital cholesteatoma (epidermoid) is often evident as a pearly white mass behind an intact tympanic membrane with no history of infection.17 They are more common in the anterosuperior quadrant of the middle ear and the posterior epitympanum. The pathophysiology for acquired cholesteatomas is thought related to TM incompetence and transposition of normal EAC epithelium into the middle ear at the time of neural tube closure.16,17

CONGENITAL DISORDERS External Auditory Canal First Brachial Cleft Cyst Branchial cleft cysts are benign congenital cysts that are remnants of the branchial apparatus. First branchial cleft cysts arise in or around the parotid gland, external auditory canal, or pinna. They may also form sinus tracts that extend from the external auditory canal to the angle of the mandible. CT demonstrates a well-circumscribed low-density cyst near the pinna, EAC, or the parotid gland. On MRI, branchial cleft cysts are

MIDDLE EAR

Inner Ear New high resolution MR sequences are particularly useful when imaging the inner ear and internal auditory meatus in the setting of SNHL. Congenital SNHL results from abnormalities of the inner ear, vestibulocochlear nerve, or CNS nuclei.18 Historically, CT has been the preferred imaging modality to delineate the osseous anatomy and congenital malformations of the inner ear. However, modern high-resolution MRI has supplanted CT as a first-line study to evaluate the membranous labyrinth, cochlea, and eighth cranial nerve.18

FIGURE 1. SWIFT imaging: SWIFT, GRE, CT, and corresponding gross pathology and histology photographs. Note the fine osseous cortical detail of the mandible provided with SWIFT demonstrating cortical erosion of the mandible, confirmed on gross pathology photograph (arrows). GRE, gradient recalled echo. Courtesy of Dr. Bevan Yueh at University of Minnesota.

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Temporal Bone Imaging

FIGURE 2. First branchial cleft cyst with fistula. Axial fat-suppressed T2 (A) and FSE T1 (B) sequences demonstrate a left preauricular unilocular T2 hyperintense cystic lesion (white arrow) with a fistula (black arrow) extending toward the external auditory canal, characteristic of a first branchial cleft cyst with fistula.

Several studies have validated the diagnostic accuracy of volumetric high-resolution heavily T2-weighted sequences. As previously mentioned, 3-D echo-balanced SSFP sequences generate high-resolution images with excellent contrast, high spatial resolution, and the ability to depict small inner ear structures.19 High-resolution submillimeter T2-weighted fast spin-echo sequences optimize visualization of the internal structures of the cochlea, such as the interscalar septum and the osseous spiral lamina.20 The volumetric MRI sequence data allow for multiplanar reformations and 3-D MIP reconstruction.20 A number of congenital inner ear anomalies have been traced to developmental insults during embryogenesis. Traditionally, congenital malformations are divided into 2 broad categories: malformations affecting only the membranous labyrinth and malformations that involve both the osseous and membranous labyrinth.17 Detection of pure membranous labyrinth anomalies are typically beyond the limits of current imaging techniques. This section will focus on a select group of malformations involving the osseous and membranous labyrinth, the diagnosis of which has been particularly facilitated by advances in MRI. The majority of these entities affect both ears asymmetrically. The following disorders represent the updated Sennaroglu and Saatci classification of the spectrum of cochleovestibular malformations that were previously grouped under the term Mondini malformation.21

Cochlear Incomplete Partition Type 2 (Classic Mondini Malformation) This represents the most common type of cochlear malformation, accounting for approximately 50% of cochlear deformities. It is less severe than IP-1 with the defect limited to the apical and middle turns of cochlea, which lack an interscalar septum and modiolus, and coalesce to form a single cystic apical cavity. The cochlea only forms 1 ½ turns with a normal basal turn; the modiolus is only present at this level. Absence of the interscalar septum and the osseous spiral lamina are best seen on thin section T2 sequences. IP-2 is always associated with an enlarged vestibular aqueduct, whereas the semicircular canals are normal.17

Cochlear Hypoplasia Cochlear hypoplasia results from abnormal development of the cochlear duct resulting in an abnormally small cochlea. It accounts for approximately 15% of cochlear malformations and lies between IP-1 and IP-2 in severity.17 In IP-1, a small cochlear bud

makes only 1 turn or less and typically arises from a small vestibule. The IAC and cochlear nerve are normal to slightly hypoplastic. A recent review by Lanferman et al described a further subclassification of hypoplastic cochlea, based on length and existence of cochlea turns, given the wide variability: Cochlear bud: severe hypoplasia with a small canal or bud representing an excrescence of the vestibule without sufficient length to form a cochlear aperture. Basal turn cochlea: only the basal turn can be identified, which is either normal width or dilated. No widely patent cochleovestibular duct is evident. Hypoplastic cochlea: basal turn is normal in length and parts of the apical turn are visualized, although reduced in size. The overall height of the cochlea is diminished.

Cochlear Incomplete Partition type 1 (Cystic Cochleovestibular malformation) IP-1 represents a completely unpartitioned cystic cochlea without any internal architecture and a dilated vestibule, which together form a “snowman” or “figure 8” appearance. The modiolus and normal internal architecture of the cochlea are absent. Often, there is an associated large IAC secondary to a defective cribiform plate, which separates the cochlea from the IAC. IP-1 is distinguished from common cavity malformation because the vestibule and cochlea can be differentiated, each maintaining their normal size.

Common Cavity Malformation This malformation results in the absence of normal differentiation between the vestibule, cochlea, and semicircular canals resulting in a single common cavity. Thin section T2-weighted images demonstrate a common fluid filled cystic cavity that may vary significantly in size, in contrast to the normal size of the cochlea and vestibule in IP-1 (Fig. 3). In addition, there is a dilated IAC and absent cochlear nerve, precluding cochlear implantation.

Labyrinthine Aplasia (Michel Aplasia) Labrynthine aplasia is the most severe and rare form of inner ear anomalies accounting for 1% of such dysplasias. It results in the complete absences of inner ear structures with a narrow atretic IAC and hypoplastic petrous apex. Magnetic resonance imaging shows a single nerve within the IAC, suggesting absence of the eighth cranial nerve. A flat appearance of the medial wall of the middle ear canal helps to differentiate from labyrinthine



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ossificans. Involvement may be unilateral or bilateral, although in unilateral cases, the contralateral side is often dysplastic. Malformations of the vestibule and semicircular canals also represent anomalies of the osseous and membranous labyrinth. Most important in this category is the enlarged vestibular aqueduct (large endolymphatic duct and sac), the most common imaging finding in patients with early onset SNHL.17 Approximately 90% of cases are bilateral, although involvement may be asymmetric, an important finding to note for surgical planning. A large percentage of patients have associated inner ear anomalies. Hearing loss tends to fluctuate in severity and may be triggered by head trauma, barometric pressure changes, or increased intracranial pressure.18 Magnetic resonance imaging reveals an enlarged endolymphatic duct and sac with a diameter exceeding the adjacent ascending portion of the posterior semicircular canal.18 In addition, there tends to be relative T2 hypointense fluid within the dilated endolymphatic sac, presumably from high protein concentration and presence of loose connective tissue.17

INFLAMMATORY AND INFECTIOUS DISEASES Inflammatory and infectious processes often necessitate CT and MRI in conjunction to evaluate complex disease processes. This section will briefly review the common infectious and inflammatory processes of the temporal bone with particular attenuation to recent advances in MRI of cholesteatomas.

Cholesteatoma As discussed previously, cholesteatomas arise from the exfoliation of hyperplastic keratinized epithelium and may be divided into congenital and acquired subtypes. Acquired cholesteatomas are the more common of the 2 types, accounting for 98% of all cholesteatomas.17 They arise from either the pars flaccida (more common) or the pars tensa of the TM. Primary acquired cholesteatomas occur in patients without a history of otitis media and are presumably related to TM retraction. Secondary acquired cholesteatomas are related to TM perforation and resultant epithelial migration into the middle ear cleft. Although the exact mechanism remains unclear, there are several theories regarding the pathophysiology of acquired cholesteatomas. Surgical resection of the epithelial matrix and debridement of the bony erosion/necrosis is the mainstay of treatment. Postoperative residual or recurrent cholesteatoma is common with a recurrence rate up to 57% after canal wall up mastoidectomy.22

CT is the first-line modality for cholesteatoma diagnosis, detailing the extent of the lesion and revealing complications, such as bony erosion.17 Pars flaccida cholesteatomas invade Prussak space and progressively erode the ossicular chain with occasional extension into the tegmen tympani and lateral semicircular canal, findings that may be readily identified on CT.16 Particular attenuation should be paid to the scutum, tympanic segment facial nerve, and tegmen tympani.23 After surgical intervention, the middle ear and mastoid are often opacified, limiting CT's ability to differentiate between granulation tissue, inflammation, infection, or recurrent cholesteatoma.16 MRI is indicated if facial nerve involvement is suspected or there is suspicion of tegmen tympani erosion with intracranial extension. In addition, MRI contributes significantly for postoperative cholesteatoma evaluation. Accurate imaging has proven useful to avoid unnecessary second-look surgery. Non-EP DWI has increased the sensitivity and specificity for detection of cholesteatoma, particularly in the postoperative setting. Contrast-enhanced T1-weighted sequences in conjunction with echo-planar diffusion-weighted sequences are helpful to differentiate granulation tissue from recurrent disease (Fig. 4). However, air-bone susceptibility of the temporal bone and middle cranial fossa produced with echo-planar diffusion sequences result in significant artifact, as discussed previously. Delayed gadolinum-enhanced T1-weighted imaging is helpful for postoperative surveillance because cholesteatomas do not enhance, whereas inflammation and granulation tissue exhibit delayed enhancement.23 However, the excellent sensitivity, specificity, and positive predictive value displayed with non-EP DWI exceeds delayed T1 postcontrast findings.16 Multiple studies have demonstrated the superiority of non-EP DWI given the diminished susceptibility artifact and cranium base distortion allowing for improved spatial resolution and therefore clearer identification of recurrent cholesteatoma (Fig. 5).24 Non-EP DWI can also be acquired at very thin slice thickness, permitting detection of cholesteatomas as small as 2 mm.23 A prospective study validated the sensitivity, specificity, and positive predictive value of non-EP DWI when compared to the gold standard of second look surgery.24

Keratosis Obturans Previously regarded as variations of the same disease, keratosis obturans (KO) and cholesteatomas are distinct entities. Keratosis obturans is the result of accumulation of desquamated keratinized material within the bony portion of the external auditory canal.25 This is typically diagnosed on CT as intraluminal soft tissue filling and widening the EAC with bony remodeling but without evidence of bony erosion; erosion is the key differentiating feature between KO and cholesteatomas. This distinction is important given the difference in management: KO is treated nonsurgically with aural toilet.26 MRI demonstrates homogenous isointense to hypointense T2 soft tissue and mild peripheral enhancement. There should be no associated reduced diffusion signal.

Chronic Otomastoiditis

FIGURE 3. Common cavity malformation. High-resolution axial T2 sequence shows a single fluid-filled cystic cavity of the inner ear without differentiation between the cochlea, vestibule, and semicircular canal.

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Chronic otomastoiditis is a long-standing inflammatory process of the middle ear and mastoid resulting in erosive changes of the middle ear ossicles. There is a strong association with chronic Eustachian tube dysfunction.17 Multiplanar CT is the best imaging modality to identify ossicular erosion. Typical findings include underpneumatization of the mastoid, erosion of the long process of the incus, widening of the incudostapedial joint, and retraction of the tympanic membrane.23 MRI adds important © 2015 Wolters Kluwer Health, Inc. All rights reserved.




FIGURE 4. Postoperative granulation tissue. Postoperative axial CT (A) shows opacification of the right middle ear (white arrow) and right mastoid. Axial T2 FIESTA image (B) reveals T2 hyperintense postsurgical signal in the right middle ear and mastoid. Axial T1 delayed postcontrast image (C) demonstrates enhancement of the soft tissue filling the surgical bed of the right middle ear and mastoid, suggestive of postoperative granulation tissue. Further evaluation with diffusion-weighted image (D) does not demonstrate reduced diffusion. Lack of reduced diffusion signal in conjunction with delayed enhancement excludes recurrent cholesteatoma. FIESTA, fast imaging using steady state acquisition.

diagnostic information in the evaluation of chronic otomastoiditis complications, such as acquired cholesteatomas, middle ear effusions, and granulation tissue (including cholesterol granuloma).23

Cholesterol Granuloma Cholesterol granuloma (CG) is a giant cell reaction to cholesterol deposits with associated fibrosis and vascular proliferation.17 This benign lesion that can occur anywhere in the air cell system of the temporal bone. CG is commonly associated with Eustachian tube dysfunction and chronic otitis media.27 Both CG and cholesteatoma can appear as expansile soft tissue masses of the middle ear. On MRI, CG demonstrates high signal on T1 and T2 spin-echo sequences and does not show reduced diffusion (Fig. 6). In contrast, cholesteatomas are characteristically T1 hypointense and T2 hyperintense.27 MRI is best at characterizing these lesions based on intrinsic signal differences and provides important presurgical information regarding local extension and complications.27

Labyrinthitis Labyrinthitis is the subacute inflammation or infection of the perilymphatic spaces of the inner ear. Inflammation within the fluid-filled spaces of the inner ear results in secondary changes of the membranous labyrinth.17 There are a variety of causes of labyrinthitis that can be classified by route of spread or infectious

agent: tympanic, meningogenic, hematogenic, posttraumatic, viral, bacterial, autoimmune, and luetic.17 Diagnosis is principally on clinical grounds, and contrast-enhanced MRI is the imaging modality of choice. In the acute and subacute stages, MRI may reveal enhancement of the perilymphatic fluid.17 Perilympathic enhancement can persist for several months after the inflammation subsides. Inflammatory enhancement tends to be less intense than that seen with intralabyrinthine tumors, such as schwannomas, which demonstrate intense, localized enhancement.28 Quantification of contrast enhancement has been advocated as an objective tool to differentiate inflammatory enhancement from tumor enhancement, which may be difficult to distinguish subjectively.28 In the early stages, normal T2 hyperintensity of the endolymph and perilymph persists, occasionally showing slightly increased signal secondary to increased cellularity. If this process of inflammation does not resolve then progression to chronic labyrinthitis results in fibrosis and eventually ossification. In the fibrous stage, MR demonstrates decreased T2 signal of the fluid filled spaces; enhancement may persist (Fig. 7). CT is useful in the late ossification phase to delineate the extent of calcified debris and ossification of the normal fluid-filled spaces.

Mucocele A mucocele is an expansile lesion of the sinuses or petrous apex secondary to complete obstruction of air cell outflow



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FIGURE 5. Postoperative evaluation for recurrent cholesteatoma. Coronal fat-suppressed T2-weighted image (A) through the temporal bone demonstrates a focal area of increased T2 signal intensity in the left middle ear cleft (white arrow). Corresponding coronal fat-suppressed T1 postcontrast image (B) shows a lack of associated enhancement (white arrow). Echo-planar DWI (C) image through the temporal bone and middle cranial fossa demonstrates marked air-bone susceptibility artefact substantially limiting evaluation for recurrent/residual cholesteatoma. Non-EP DWI (D) reveals reduced diffusion and confirms the presence of recurrent/residual cholesteatoma due to improved spatial resolution and decreased susceptibility artefact.

with mucous secretions.17 It is associated with long T1 and T2 relaxation times although the signal intensity can vary significantly depending on the chronicity and protein levels.29

INFECTION Necrotizing Otitis Externa Acute external otitis is a bacterial infection of the external auditory canal. Diagnosis is typically made on clinical grounds. Necrotizing otitis externa (NOE), previously known as malignant otitis externa, is an aggressive subtype of otitis externa typically seen in diabetic and immunocompromised patients. The NOE progresses from soft tissue cellulitis to chondritis and eventually osteomyelitis.23 The infection extends through the fissures of Santorini and the tympanomastoid suture from the osseous EAC into the mastoid as well as the TMJ and petrous apex.17,23 In advanced cases, intracranial extension and dural sinus thrombosis may occur. Central skull base involvement and intracranial extension may be seen via spread along the vascular and fascial planes; multiple cranial neuropathies may result.17,30 Facial nerve involvement, when present, occurs at the level of the stylomastoid

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foramen. The MRI findings include retrocondylar fat infiltration, parapharyngeal wall thickening, preclival soft tissue infiltration, skull base and condylar bone marrow infiltration, masticator space infiltration, and dural enhancement of the middle and posterior cranial fossa (Fig. 8).30 Because of a fibrotic necrotizing process, in contradistinction to other inflammatory diseases, NOE shows low signal intensity of the soft tissue changes on both T1- and T2weighted sequences.23 Surrounding T2 hyperintense edema may be seen from inflammatory changes of the middle ear, mastoid, and skull base. Postcontrast imaging demonstrates dural enhancement and dural sinus filling defects if thrombosis is present.

Apical Petrositis The petrous apex, the most anterior and medial portion of the temporal bone, is not pneumatized in most adults. Patients with a pneumatized petrous apex are subject to infectious and inflammatory complications via communication of the air cells with the mastoid and middle ear.17,31 Apical petrositis should be suspected in suppurative ear infection with persistent deep-seated pain. It can occur with or without concurrent mastoiditis.31 The disease process is similar to coalescent mastoiditis, resulting in the © 2015 Wolters Kluwer Health, Inc. All rights reserved.




FIGURE 6. Petrous apex cholesterol granuloma. Axial T1 (A) and T2-weighted (B) images show a left petrous apex mass demonstrating high T1 (white arrow) and T2 signal intensity. The DWI ADC map (C) and trace image (D) demonstrates facilitated diffusion, excluding a cholesteatoma.

coalescence of the pneumatic cells and destruction of bony septa.31 In this setting, CT reveals opacification of the petrous apex air cells. Contrast-enhanced MRI demonstrates inflammatory changes within the petrous apex and intracranial complications, if present.

Cortical destruction can result in epidural abscesses, meningitis, empyema, and cranial neuropathies. It should be noted that benign debris is commonly seen in asymptomatic patients and should not be confused with petrositis.

FIGURE 7. Labyrinthitis-fibrous stage. Axial T2 FLAIR (A) image demonstrates subtle abnormal signal of the left vestibule (white arrow). Axial T2 FIESTA (B) image demonstrates asymmetric loss of normal T2 hyperintense signal (black arrow) of the perilymphatic fluid of the left inner ear structures. © 2015 Wolters Kluwer Health, Inc. All rights reserved.


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FIGURE 8. Necrotizing Otitis externa. Coronal fat-suppressed T2 (A) and axial fat-suppressed T1 postcontrast images (B) reveal extensive middle ear and mastoid fluid and marked transpatial enhancement. Enhancement involves the EAC, periauricular soft tissues and extends into the right masticator space.

Bell Palsy (Idiopathic Facial Paralysis) Bell palsy describes the clinical entity of acute onset lower motor neuron facial paralysis. The cause often remains idiopathic but may be related to herpes virus reactivation from the geniculate ganglion.32 Inflammation of the nerve results in swelling and entrapment within the bony facial canal, resulting in nerve dysfunction. Many patients complain of a viral prodrome or simultaneous alterations in taste due to chorda tympani dysfunction. Contrast-enhanced MRI demonstrates uniform enhancement of an otherwise normal facial nerve (Fig. 9). Swelling of the nerve is atypical. Nodular enhancement or focal thickening should not be seen, an important feature in distinguishing inflammatory enhancement from neoplasm. Some enhancement of the facial nerve is normal on MR. Enhancement can be seen in the perigeniculate segment and in the tympanic segment of the nerve. Facial neuritis is suggested when there is asymmetric enhancement of the facial nerve originating at the fundus of the IAC, within the labyrinthine and tympanic segment and occasionally seen extending to the level of the stylomastoid foramen.17,23 The duration of enhancement is variable but may be persistent for several months after clinical remission. It is important to note that not all patients with a clinical syndrome of Bell palsy demonstrate abnormal facial nerve enhancement.33

Otomastoidits Acute otomastoiditis is a bacterial infection of the middle ear that typically develops in a child with Eustachian tube dysfunction. Inflammation and effusion within the middle ear cleft result in mucosal swelling, often blocking the aditus ad antrum and resulting in trapped mastoid secretions. In mild acute cases, the disease is well controlled with antibiotics. However, inadequately treated infections may result in serious complications, such as coalescent mastoiditis, subperiosteal abscess, meningitis, empyema, and dural sinus thrombosis. Coalescent mastoiditis is the consequence of persistent infection resulting in osteoclastic resorption of the mastoid trabeculae with air cells coalescing into an irregular cavity. Given variability in mastoid pneumatization, comparison with the contralateral side is helpful to detect trabecular breakdown. A subperiosteal abscess may result from extension through the mastoid cortex. A Bezold abscess is a type of subperiosteal abscess that occurs when infection erodes

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through the mastoid tip medial to the insertions of the sternocleidomastoid and posterior belly of the digastric muscle.31 Inflammatory debris may extend inferiorly in the posterior cervical space, deep to the sternocleidomastoid muscle.17,31 Both CT imaging and MRI can diagnose a Bezold abscess; however, CT is better to evaluate for associated periostitis, trabecular breakdown, and cortical erosion (Fig. 10). Less common complications, such as meningitis and dural sinus thrombosis, are best evaluated with contrast enhanced MRI.

VASCULAR ANOMALIES Aberrant Internal Carotid Artery Aberrant internal carotid artery (ICA) is a congenital vascular anomaly resulting from agenesis of the first extracranial segment of the ICA (C1) with arterial collateral pathway formation. There is resultant enlargement of the collateral ascending pharyngeal and inferior tympanic arteries. The normal endocranial opening of the carotid canal does not develop, and there is resultant hypertrophy of the interior tympanic canaliculus.17,34 This aberrant pathway results in posterolateral displacement of the petrous carotid canal. The aberrant ICA courses anteriorly along the cochlear promontory to anastomose with the horizontal portion of the petrous ICA through a dehiscence in the carotid plate.17 Diagnosis can be made with unenhanced temporal bone CT, CTA, or MRA (Fig. 11). Identifying an aberrant carotid has obvious surgical implications and may result clinically in pulsatile tinnitus.34

Persistent Stapedial Artery Persistent stapedial artery is a rare congenital vascular anomaly, often asymptomatic and incidentally diagnosed on crosssectional imaging or during middle ear surgery. The stapedial artery arises from the vertical petrous ICA, enters the anteromedial hypotympanum and is contained within an osseous canal.35,36 It then leaves the canal at the cochlear promontory and courses dorsally and cephalad through the obturator foramen of the stapes into the facial canal and travels anteriorly, exiting before the geniculate ganglion.36 The stapedial artery then gives rise to the medial meningeal artery within the dura of the middle cranial fossa. PSAs may occur with or without an aberrant ICA. As with most other vascular anomalies, diagnosis can be made with CTA or MRA; © 2015 Wolters Kluwer Health, Inc. All rights reserved.




FIGURE 9. Bell palsy: Coronal (A) and axial (B) fat-suppressed T1 post-contrast sequences demonstrate smooth enhancement of the intracanalicular (white arrow), labyrinthine and tympanic (black arrow) segments of the right facial nerve.

however, occasionally, the artery is too small to resolve on MRA. Associated findings include the absence of a normal foramen spinosum. Identification of a persistent stapedial artery is relevant in the evaluation of pulsatile tinnitus or preoperative planning for middle ear surgery.

High/Dehiscent Jugular Bulb A normal jugular bulb lies inferior to the posterior aspect of the floor of the middle ear.37 Two common clinically relevant variants of temporal bone venous anatomy include a high jugular

FIGURE 10. Bezold abscess—complication of coalescent otomastoiditis. Axial T2-weighted (A) image show abnormal right mastoid T2 hyperintense signal and abnormal right sigmoid sinus flow void (white arrow), consistent with venous sinus thrombosis. Contrast-enhanced axial (B) and coronal (C) T1-weighted images demonstrate several small peripherally enhancing collections (black arrows) within the soft tissues inferior to the mastoid tip and posterolateral neck. (D) Corresponding reduced diffusion signal (gray arrow) is present with corresponding reduced ADC values (not shown), confirming the presence of a multiloculated abscess. © 2015 Wolters Kluwer Health, Inc. All rights reserved.


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Petrous ICA Aneurysm Vascular lesions of the extradural petrous segment ICA are rare. The petrous ICA is often sparred pathologically because of its protected course through the carotid canal, minimal atherosclerotic change, and absence of branch points for aneurysm formation. Although rare, the petrous ICA is vulnerable to pseudoaneurysm formation in the setting of trauma or dissection given the fixed nature of the petrous segment relative to the more mobile proximal cervical segment.39 Computed tomography demonstrates an expansile petrous mass with smooth bony margins. On MRI, pseudoaneurysm may mimic a mucocele or CG.40 CTA and MRA are diagnostic; however, catheter angiography remains the gold standard (Fig. 13). The management of these lesions remains challenging as the location within the bony carotid canal makes open surgical repair difficult. Recent advances in endovascular therapy have become the treatment modality of choice.

TEMPORAL BONE NEOPLASMS Meningioma FIGURE 11. Aberrant internal carotid artery. Time-of-flight MRA with source images (A) and 3-D reformation (B) demonstrate abnormal course and size of the right ICA that is displaced posterolaterally into the middle ear (white arrows).

bulb and a dehiscent jugular bulb. The definition of a high jugular bulb can vary slightly in the literature. In general, it occurs when the superior aspect of the jugular bulb extends above the floor of the IAC and is more commonly seen on the right side (Fig. 12).38 A dehiscent jugular bulb results in superior and lateral displacement of the jugular bulb into the middle ear cavity through a dehiscent sigmoid plate. The dehiscent jugular bulb can be seen behind the posteroinferior quadrant of the tympanic membrane on otoscopic examination.17 As with the previously discussed vascular variants, high and dehiscent jugular bulbs have been linked to symptoms of pulsatile tinnitus and should be included in the differential diagnosis of a retrotympanic vascular mass. High and dehiscent jugular bulbs can be diagnosed with CT or MRI. The main differentiating features are whether the sigmoid plate is intact and if there is protrusion into the middle ear.

Meningiomas are derived from arachnoid meningoepithelial cells.41 They are well-circumscribed, broad-based extra-axial tumors arising from the dura. Most arise from the dura of the posterior petrous wall and are identified at the cerebellopontine angle (Fig. 14).41,42 Meningiomas that arise from the tegmen tympani and jugular foramen commonly invade the middle ear cavity. Primary IAC meningiomas are extremely rare. On CT, meningiomas are described as soft tissue density lesions that are isoattenuating/hyperattenuating to brain parenchyma.42,43 Meningiomas classically cause hyperostosis of adjacent bone that is best visualized on CT as irregular osseous thickening with spiculated margins.42,44 Meningiomas are typically isointense on both T1- and T2-weighted images but demonstrate variable signal intensity. A characteristic thin cleft of CSF signal intensity may be seen surrounding the tumor. Signal voids representing diffuse mineralization and cystic foci can also be seen.42 Meningiomas show avid homogenous enhancement with gadolinium and intense enhancement of an adjacent linear “dural tail” is characteristic. Cholesteatomas, in contrast, do not enhance. T2 hyperintense edema can also be seen in peritumoral brain parenchyma.44 Tegmen tympani and jugular foramen meningiomas that have invaded the middle ear cavity can be differentiated from

FIGURE 12. High jugular bulb without dehiscence. Coronal noncontrast CT (A) and axial SPGR postcontrast images (B) show a high-riding enlarged jugular bulb, which extends above the floor of the IAC (white arrows). High and dehiscent jugular bulbs occur more commonly on the right, as seen in this case. Note that the sigmoid plate is intact (black arrow), differentiating a high jugular bulb from a dehiscent jugular bulb.

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FIGURE 13. Petrous carotid aneurysm. Time-of-flight MRA with 3-D reformation (A) and axial source image (B) demonstrate a lateral out-pouching of the right petrous internal carotid artery consistent with a saccular aneurysm.

FIGURE 14. CPA meningioma. Classic left cerebellopontine angle meningioma (white arrow) demonstrating mildly increased T2 signal (A), T1 isointense signal (B) and avid uniform enhancement on postcontrast images (C, D). Note there is a thin rim of CSF (“CSF cleft”) between the meningioma and the left cerebellar hemisphere, confirming that this is an extra-axial mass (black arrow). © 2015 Wolters Kluwer Health, Inc. All rights reserved.


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glomus tumors by the absence of vascular flow voids on MRI and their tendency to encase the ossicular chain.

Schwannomas Schwannomas of the temporal bone are benign, slow-growing tumors derived from the perineural Schwann cells of CN V, VII, and VIII (Fig. 15).41 Rarely, vestibular schwannomas associated with NF1 undergo malignant degeneration. Schwannomas are classically isoattenuating to brain parenchyma on CT, hypointense on T1-weighted and hyperintense with cystic components on T2-weighted sequences (Fig. 16).45 Schwannomas uniformly show avid enhancement. Specific imaging considerations for facial schwannomas, vestibular schwannomas, and intralabryntine schwan nomas will be discussed. Trigeminal schwannomas are uncommon in the temporal bone, becoming relevant only with extension into the petrous apex from its origin in Meckel's cave.45 Vestibular schwannomas commonly arise from the vestibular ganglion near the fundus of the IAC. They present with SNHL. On CT, schwannomas can be found anywhere along the nerve from IAC to the vestibule, cochlea, or semicircular canals.46 Vestibular schwannomas classically cause enlargement of the porous acousticus in contrast to cerebellopontine meningiomas.42,45 Vestibular schwannomas can be entirely intracanalicular or intracisternal.41 A characteristic finding on post-contrast T1 is the “ice cream on cone” appearance created by a small intracanalicular component in the IAC lateral to a large cisternal component. Magnetic resonance imaging is the preferred imaging modality for evaluating small tumors undetectable on CT.

High-resolution T2-weighted images are excellent at revealing hypointense filling defects measuring only a few millimeters within the normal high CSF signal intensity of the IAC and cistern.41 Intralabyrinthine schwannomas arise from the intralabyrinthine branches of CN VIII and like vestibular schwannomas, also present with SNHL. They are further subdivided by location: intracochlear, intravestibular, and vestibulocochlear refer to tumors confined to the cochlea, vestibule, or both, respectively. Transmacular, transmodiolar, and transotic refer to tumors that have achieved minor extension into the IAC. As with vestibular schwannomas, high-resolution T2-weighted images reveal hypointense filling defects within the normal high CSF signal intensity of the intralabyrinthine fluid, allowing for detection of tumors as small as 2 to 3 mm otherwise undetectable on CT.46 Additionally, increased protein content in peritumoral fluid decreases the T2 FLAIR signal in the membranous labyrinth.42 Although schwannomas may appear slightly hyperintense to normal perilymph on T1-weighted images, better visualization is achieved after gadolinium administration. Labrynthitis, which also shows uniform enhancement in the membranous labyrinth, does not share the T2 findings of schwannomas.46 Facial nerve schwannomas are slightly more complex as they may involve a single segment or multiple segments of CN VII as it courses through the temporal bone. Large facial schwannomas are easily identified on CT as expansile, well-circumscribed, fusiform lesions that cause smooth remodeling of the surrounding bony canal. They can have a “tubular” or “sausage-link” appearance depending on the pattern of segment involvement.42 They demonstrate heterogeneous enhancement in the signal void of the temporal bone. Facial nerve schwannomas arising from the

FIGURE 15. Small intracanalicular schwannoma. (A) Axial T2 FIESTA sequence shows hypointense signal in the right IAC (white arrow). Axial (B) and coronal (C) fat-suppressed T1 post-contrast images (white arrows), and axial DWI (D) show avid enhancement of a small intracanalicular mass, which does not restrict diffusion.

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FIGURE 16. Facial nerve schwannoma. Axial CT (A) demonstrates significant enlargement of the anterior genu and proximal tympanic segment of the facial nerve canal (white arrow). Axial T1-weighted image (B) demonstrates mild increased T1 signal intensity (black arrow) and substantial enlargement of the tympanic segment of the facial nerve with avid enhancement (black arrow) on T1 postcontrast image (C).

IAC can compress CN VIII, leading to sensineural hearing loss and clinically mimicking vestibular schwannomas. Parasagittal reformations of a high-resolution 3-D T2-weighted sequence are useful in differentiating the 2 entities by localizing the lesion in the IAC to either the anterosuperior quadrant with a facial nerve schwannoma or posteroinferior quadrant with a vestibular nerve schwannoma.44 Tympanic segment schwannomas that invade the middle ear can compress the ossicles to cause CHL, thereby mimicking meningiomas.44

Paragangliomas Paragangliomas are the most common neoplasm of the middle ear and the second most common in the temporal bone.42 They are benign lesions derived from the extra-adrenal neural crest paraganglia or “glomus bodies.”44 Pulsatile tinnitus with a middle ear mass on otoscopic examination is the most common clinical presentation.44 They can be sporadic or associated with MEN 2A/AB.42 Paragangliomas are subdivided into 3 distinct types, depending on the nerve and location from which they arise. Glomus tympanicum tumors are confined to the tympanic cavity and arise along the cochlear promontory from Jacobson nerve, the inferior tympanic branch of CN IX. These tumors manifest with clinical symptoms early on and are therefore relatively small at presentation.42 Glomus jugulare tumors are confined to jugular bulb and skull base and arise from Arnold nerve, the mastoid branch of CN X. Glomus jugulotympanicum tumors share components of both glomus tympanicum and glomus jugulare (Fig. 17). Computed tomography is a good initial imaging choice to evaluate anatomic location. Small glomus tympanicum tumors are identified as soft tissue densities situated anteriorly in the hypotympanum against the cochlear promontory. Larger lesions can fill the entire middle ear cavity with retained fluid opacification in the mastoid.41,44 Although glomus tympanicum tumors do not cause osseous erosion, the more aggressive glomus jugulotympanicum tumor demonstrates an infiltrative, permeative erosion of the jugular foramen and skull base.44 Paragangliomas are classically hypointense on T2 and hyperintense on T2-weighted imaging. Tumors larger than 2 cm have a characteristic “salt and pepper” appearance on unenhanced T2weighted sequences where the pepper represents high-velocity signal flow voids of large feeding arteries and the salt represents foci of intratumoral hemorrhage.41,42,45 Glomus tumors show strong enhancement in the signal void of the temporal bone

comparable to that of the adjacent ICA. As paragangliomas are known to travel along paths of least resistance, MRI is useful in defining intracranial extension into the skull base as well as the petrous bone, which occurs via preformed air cell tracts.41,45 Magnetic resonance imaging also helps identify important neurovascular relationships, for example, encroachment of the carotid artery, or intravascular growth within the jugular vein leading to venous occlusion.47 Finally, MRI is a valuable tool in differentiating expected postsurgical change from tumor recurrence. Because glomus tumors are hypervascular, MRA is used to evaluate the presence of collateral blood supply and in preoperative embolization. Serpiginous, intratumoral high-signal intensities seen on time-of-flight MRA reflect the high-velocity flow of feeding arteries.41,42Contrast-enhanced-MRA (elliptical centric contrast-enhanced MRA) is superior when used with conventional MR compared to conventional MR alone. Findings of an intense tumor blush and early draining veins have 100% sensitivity and 94% specificity for diagnosing paragangliomas. Additional advantages of contrast-enhanced MRA over conventional MR are faster acquisition time and a larger field of view extending from aortic arch to skull base.48

Squamous Cell Carcinoma Primary tumors of the external ear involving the external auditory canal and the mastoid bone include squamous cell, basal cell, melanoma, lymphoma, myeloma, osteosarcoma, and chondrosarcoma. The most common primary malignant tumor of the external auditory canal is squamous cell carcinoma (SCC), which is associated with therapy-resistant chronic external and middle ear infections.42,44 SCC demonstrates aggressive bone destruction, often invading the temporomandibular joint, parotid gland, carotid canal, and middle ear.42 No universally accepted staging system exists for temporal bone tumors. However, application of the Pittsburgh Staging System for SCC in the external ear relies heavily on MR findings of soft tissue invasion, extension into middle ear and mastoid, and involvement of cranial nerves.

Endolymphatic Sac Tumors Endolymphatic sac tumors (ELST), also known as invasive papillary cystadenomatous tumors, are very rare neoplasms that arise from the epithelium of the endolymphatic sac near the vestibular aqueduct in the retrolabyrinthine petrous bone.41,42 They



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FIGURE 17. Glomus jugulare. Precontrast (A) and postcontrast (B) axial CT images show an expansile enhancing mass arising from the jugular foramen with resultant permeative osseous destruction (white arrows). The soft tissue mass appears to erode into the inner ear. Axial T1-weighted image (C) shows scattered areas of signal hypointensity (black arrow), consistent with vascular flow voids, the “salt-and-pepper” appearance. Axial MRA source image (D) confirms extensive associated vascularity (black arrow).

Metastatic Disease

manifest clinically with unilateral hearing loss and tinnitus and may occur sporadically or in association with VHL. On CT, ELSTare soft tissue masses that appear “moth-eaten” and permeative with aggressive margins causing erosion of the posterior petrous bone. Large lesions greater than 3 cm often invade the middle ear, cerebellopontine angle and jugular foramen.41 Computed tomography reveals characteristic intratumoral bone spicules representing sequelae of lytic destruction.41,42 The ELST tumors are hypervascular receiving blood supply from the external carotid artery, specifically the distal branches of the ascending pharyngeal and occipital arteries.41,49 On MRI, ELST exhibit variable T1 and T2 signal intensity with both solid and cystic components, as well as heterogeneous enhancement patterns.41,42 Foci of high T1 signal reflecting methemoglobin deposition from frequent intratumoral subacute hemorrhage are seen peripherally in smaller tumors and diffusely within larger tumors (Fig. 18).42,45 Despite its hypervascularity, only tumors larger than 2 cm show characteristic flow voids.49

Metastatic disease in the temporal bone occurs most often in breast cancer.41,45 The petrous portion of the temporal bone is a frequent site of metastasis via a hematogenous route, secondary to slow blood flow through petrous apex marrow that allows for filtering and deposition of tumor cells.45 Other malignancies that metastasize to the temporal bone include lung, prostate, and renal cell carcinoma. Metastasis can occur by direct extension as in nasopharyngeal carcinoma as well as by leptomeningeal extension. Metastatic tumors exhibit relatively nonspecific imaging characteristics with variable MR signal intensity and enhancement patterns. Additionally, intratumoral flow voids seen on MR in highly vascular metastases like renal cell, melanoma, and thyroid cancer may mimic other hypervascular temporal bone tumors, such as paragangliomas.45 As with the staging of primary temporal bone cancers, MR is essential in defining soft tissue invasion, intracranial extension, and involvement of neurovascular structures.

Chondrosarcomas

Perineural Tumor Spread

Chondrosarcomas are one of the few malignant tumors in the temporal bone. They are the most common tumor seen at the petrous apex, occurring along the petrosphenoidal and petrooccipital synchondroses.42 On CT, chondrosarcomas demonstrate bony destruction with rings of calcification.45 Chondrosarcomas are classically hypointense on T1-weighted and hyperintense on T2-weighted images with a variable, heterogeneous enhancement pattern.

Perineural spread of tumor describes a form of metastasis seen in head and neck cancers in which tumors disseminate to noncontiguous regions along a nerve or nerve sheath.50 In the temporal bone, the facial nerve is most often implicated in the perineural spread of salivary gland tumors and skin malignancies that secondarily invade the parotid gland.42 Although the pattern of spread predictably follow the course of the nerve, “skip lesions” or areas of uninvolved or microscopically involved nerve between

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FIGURE 18. Endolymphatic sac tumor. Axial T1-weighted (A) and gradient echo (B) images demonstrate a heterogeneous mass in the left inner ear with extension to the cerebellopontine angle (black arrow). Intrinsic T1 shortening is compatible with hemorrhage, characteristic of endolymphatic sac tumors. (C) Axial T1 postcontrast image reveals extensive associated enhancement (white arrow).

bulky tumor growth can make the diagnosis less conspicuous.50 An important CT finding is segmental enlargement or destruction of a foramen or bony canal. However, because the facial nerve is normally much smaller in diameter than its surrounding foramen, nerve enlargement to the point of causing osseous destruction takes time, making this a delayed CT finding. Magnetic resonance imaging is therefore a preferred imaging modality because

of its multiplanar capability, superior soft tissue contrast, and decreased artifact from dental hardware.50 On T1 fat-suppressed images, abnormal nerve thickening and enhancement can be seen early in the disease course (Fig. 19). Eventually, neuropathic atrophy is seen. Coronal reformatting improves visualization of the nerve as it courses through foraminal openings, such as the stylomastoid foramen. This is an important location to look for

FIGURE 19. Delayed perineural tumor spread status post resection of a parotid adenocarcinoma. Preoperative fat-suppressed T1 post-contrast image (A) demonstrates an irregular enhancing parotid mass that extends into the deep lobe of the parotid gland (black arrows). Follow-up postsurgical axial fat-suppressed T2 (B), axial (C) and coronal (D) fat-suppressed T1 postcontrast images show abnormal thickening and enhancement of the genu and tympanic segments of the facial nerve with extension along stylomastoid foramen (white arrows). © 2015 Wolters Kluwer Health, Inc. All rights reserved.


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obliteration of fat planes that would suggest replacement with tumor.50 Because most cases are clinically asymptomatic, any of these MR findings should raise the suspicion for perineural tumor spread in a patient with a history of cancer, even if the primary tumor has been treated.42

14. Kendi AT, Khariwala SS, Zhang J, et al. Transformation in mandibular imaging with sweep imaging with Fourier transform magnetic resonance imaging. Arch Otolaryngol Head Neck Surg. 2011;137:916–919.

Rhabdomyosarcoma

16. de Moura MVT, de Lima Taranto DO, de Mattos Garcia M. Cholesteatoma: utility of non-echo-planar diffusion-weighted imaging. Radiol Bras. 2012;45:283–287.

Rhabdomyosarcomas are the most common primary temporal bone malignancy and affect young children.45 They arise from either intrinsic middle ear musculature or primitive pluripotential mesenchymal remnants.44 Typical clinical presentation is chronic otitis media with a sudden onset of facial palsy. Tumors characteristically involve the external auditory canal and middle ear from which medial extension to the petrous apex is common.45 The CT imaging reveals an aggressive soft tissue mass causing extensive osseous destruction. On MR, rhabdomyosarcomas show intermediate T1 and variable T2 signal intensity. Replacement of the normal fat signal and middle ear signal voids with soft tissue strongly enhances its characteristic.44 REFERENCES 1. Bagai A, Thavendiranathan P, Detsky AS. Does this patient have hearing impairment? JAMA. 2006;295:416–428. 2. Angtuaco EJ, Wippold II FJ, Cornelius RS, et al. ACR appropriateness criteria hearing loss and/or vertigo. Available at https://acsearch.acr.org/ docs/69488/Narrative/. American College of Radiology. Accessed September 3, 2014. 3. Sauvaget E, Kici S, Kania R, et al. Sudden sensorineural hearing loss as a revealing symptom of vestibular schwannoma. Acta Otolaryngol. 2005; 125:592–595. 4. Kano K, Tono T, Ushisako Y, et al. Magnetic resonance imaging in patients with sudden deafness. Acta Otolaryngol Suppl. 1994;514:32–36.

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Osteoradionecrosis of the temporal bone.

Temporal bone histopathology of osteopetrosis.

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Chemodectomas involving the temporal bone.

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Temporal bone histopathology: residents' quiz.

Optimal Imaging Parameters for Readout-segmented EPI of the Temporal Bone.

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CT Imaging of Temporal Bone Chondroblastoma: A Report of Two Cases.

Temporal imaging with squeezed light.

En bloc resection of the temporal bone and temporomandibular joint for advanced temporal bone carcinoma.

A new temporal bone and cadaver head holder for temporal bone surgical technique training.

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Desmoplastic Fibroma of the Temporal Bone.

Treatment outcomes of temporal bone osteoradionecrosis.

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